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2017 ; 14
(4
): 4619-4624
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Role and mechanism of action of LRIG1 in ovarian cancer cell line and VP16
drug-resistant cell line
#MMPMID28943962
Zhang Y
; Liu Z
; Yu S
Oncol Lett
2017[Oct]; 14
(4
): 4619-4624
PMID28943962
show ga
We investigated the role of leucine-rich repeats and immunoglobulin-like domains
(LRIG)-1 in ovarian cancer cell line and VP16 drug-resistant cell line to explore
the possible mechanism of action. Human ovarian cancer cell line SKOV3 and the
VP16 drug-resistant cell line SKOV3/VP16 were used to investigate whether LRIG1
affects the sensitivity of SKOV3 to drugs. RT-qPCR was used to detect the
difference in LRIG1 expression between drug-resistant and wild-type cell lines.
siRNA LRIG1 was designed and transfected to silence LRIG1 to investigate the
mechanism by which LRIG1 affects the sensitivity of SKOV3 to drugs. Wild-type
cells were transfected with SKOV3. The cells were divided into 3 groups (VP16, NC
+ VP16 and siRNA LRIG1 + VP16 treatment group). VP16 (IC(50) value) was added 24
h after transfection. The CCK-8 method was used to detect the proliferation of
each group at multiple time points (0, 24, 48 and 72 h). A colony-forming assay
was used to detect cell proliferation and flow cytometry was used to detect cell
apoptosis. The expression of LRIG1 was lower in the drug resistant cell line than
that of the wild-type cell line. The expression of LRIG1 significantly decreased
with the increase of VP16 concentration (P<0.05). The apoptotic rate was
decreased but there was an increase on cell clones in the siLRIG1 + VP16-treated
group as compared to VP16- and NC+ VP16-treated groups (P<0.05). The LRIG1 gene
affects the sensitivity of SKOV3 cells to drug in a dose-related manner,
indicating that the reduced expression of LRIG1 can inhibit cell apoptosis.